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Toxicology > Cyanide (FINAL) > Flashcards

Cyanide (FINAL) Flashcards

1
Q

Which species are most likely to get cyanide poisoning?

A

Large animals

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2
Q

What are possible sources of cyanide poisoning in large animals?

A
  • Ingestion of cyanogenic plants
    • Wild cherry (Prunus spp)
    • Sudan grass, Johnson grass, and sorghums
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3
Q

What does sudan grass, Johnson grass, and sorghum contain?

A

Cyanogenic glycosides that can liberate toxic amounts of HCN

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4
Q

What species is this?

A

Chokecherry (Prunus spp)

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5
Q

What is this?

A

Sorghums (Sorghum spp)

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6
Q

What can be a source of cyanide poisoning in small animals?

A

Hydrogen cyanide and cyanide salts have many uses that lead to poisoning in small animals

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7
Q

What is used as a fumigant rodenticide that can cause poisoning in small animals?

A

Hydrogen cyanide gas

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8
Q

What compound do some fertilizers contain that is toxic to small animals?

A

Cyanamide

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9
Q

T/F: Sodium nitroprusside is used as a hypotensive

A

TRUE

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10
Q

Combustion of what produces HCN gas that can poison small animals?

A

Many plastic compounds

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11
Q

What are some cyanogenic plants that cause toxicity in small animals?

A
  • Prunus spp
    • Cherries, apples, plums, apricots
  • Some species of lima bean and cassava roots (tapioca)
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12
Q

What is cyanide also known as?

A

Hydrogen cyanide (HCN), hydrocyanic acid, or prussic acid

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13
Q

Is HCN a volatile gas?

A

YES

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14
Q

T/F: HCN will disappear as the plant dries and also from the rumen contents

A

TRUE

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15
Q

What is HCN’s characteristic odor?

A

Bitter almond or ammoniacal

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16
Q

Is HCN an irritant to mucous membranes

A

Of course it is

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17
Q

What does the CN- radical form?

A

Complexes with a number of chemicals, such as ferric ion, cupric, and molybdenum

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18
Q

Does cyanide have an antithyroid effect?

A

No–thiocyanate SCN has an antithyroid effect

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19
Q

What are the toxic levels of cyanide?

A

Greater than 200ppm in the plant is toxic

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20
Q

What is the acute oral MLD of HCN?

A

2-2.3 mg/kg in all species

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21
Q

Which species are more/less susceptible to cyanide toxicosis?

A
  • Ruminants are more susceptible than horses and swine
  • Sheep are less susceptible than cattle
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22
Q

Why are ruminants more susceptible to HCN poisoning?

A

Hydrolysis by the rumen microflora causes release of cyanide from cyanogenic plants

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23
Q

What happens to cyanogenic plants when damaged?

A
  • Plant damage (stunting, wilting, trampling, frost, drought, or treatment w/ 2,4-D herbicides)
    • Causes release of beta-glucosidase that causes hydrolysis of cyanogenic glycosides and release of cyanide (HCN)
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24
Q

What is the order of cyanogenic glycoside concentrate in plant parts?

A

Seeds > leaves > bark > stems > fruit

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25
Q

Which plant stage contains more glycoside?

A

Young/growing

26
Q

What soil condition might increase cyanide poisoning?

A

High N or low P–may increase glycoside

27
Q

T/F: Plants can contain large amounts of free HCN and cyanogenic glycoside

A

TRUE

28
Q

T/F: Rapid ingestion and ingestion of large portions of a cyanogenic plant can cause toxicosis

A

TRUE

29
Q

Where is HCN absorbed from?

A

HCN is rapidly absorbed from the GI tract, by inhalation, and from intact skin

30
Q

Where is HCN distributed?

A

Throughout the whole body

31
Q

Where is CN- metabolized?

A

In the presence of thiosulfate, CN- is metabolized by serum and liver sulfurtransferase (rhodanese) to thiocyanate (SCN-) which is relatively less toxic and is excreted in the urine

32
Q

Excretion of HCN?

A

Small amounts are excreted in the urine or expired air

33
Q

What happens to excess CN- in tissues/blood?

A

It binds with ferric iron and cupric copper of the mitochondrial cytochrome oxidase

–> this blocks electron transport and inhibits the cells from utilizing available oxygen –> histotoxic anoxia particularly in the brain

34
Q

Does CN- toxicosis respond to oxygen therapy

A

NO–cells can’t utilize the available oxygen

35
Q

T/F: Anaerobic glycolysis leads to metabolic acidosis in HCN toxicosis

A

TRUE

36
Q

What might cyanide inhibit following toxicosis?

A

May inhibit enzymes of glycolysis and citric acid cycle and decrease cellular energy

37
Q

What effect does cyanide have?

A

A prominent vasoconstrictor effect

38
Q

Does HCN toxicosis cause neuronal damage?

A

Yes, due to histotoxic anoxia

39
Q

What occurs following chronic HCN toxicity?

A
  • Neuronal degeneration and demyelination of the spinal cord and brain
  • Low levels of cyanide are goitrogenic due to thiocyanate
40
Q

T/F: Both peracute and acute poisoning can have an extremely rapid onset

A

TRUE

41
Q

T/F: Animals may die from poisoning without manifesting clinical signs

A

TRUE

42
Q

What are the clinical signs of acute poisoning?

A
  • Signs occur in rapid succession and include tachypnea, apparent anxiety, severe panting, gasping, and behavioral alarm
  • Other signs may be muscle tremors, salivation, lacrimation, urination, defecation, severe colic, vomiting, prostration, bright red mucous membranes (from hyperoxygenation of the blood), clonic convulsions, and rapid death
43
Q

T/F: Signs of acute HCN poisoning will vary among species

A

FALSE–signs are similar in all species

44
Q

How long does it take for animals to die from acute poisoning?

A

About 4-5min from onset of clinical signs

45
Q

What are the clinical signs of chronic poisoning?

A
  • Posterior paralysis, urinary incontinence and cystitis, which may result in infection
  • Constipation due to lower spinal cord degeneration
  • May have goitrogenic effect
46
Q

Which sample is positive for cyanide poisoning?

A

Far left

47
Q

What are the lesions associated with cyanide toxicosis?

A
  • Bright red mm, cherry-red blood that may not clot or will slowly clot
  • GI tract and lungs show congestion and petechial hemorrhages
  • Plants may be seen in rumen contents
  • May be smell of cyanide, although it leaves the rumen contents rapidly
48
Q

What specimens are used for chemical analysis?

What should be done to the specimens?

A
  • Forage (200ppm considered toxic), blood (stays longer than in tissues), rumen contents, liver, muscle, brain, and heart (if taken w/in 4hrs of death)
  • Brain and heart are good specimens
  • All specimens (except blood) should be frozen immediately and kept frozen until analysis
49
Q

What can be used as a preservative for plant specimens?

A

Adding 1-3% solution of mercuric chloride–prevents hydrolysis

50
Q

Is chemical analysis useful for emergency situations?

A

No–results take days

51
Q

What is elevated on the lab diagnosis?

A
  • Elevated thiocyanate levels in urine
  • Lactic acidosis and increased anion gap
    • Good indicators for presence and severity of cyanide poisoning
52
Q

What is the sodium picrate paper test?

A
  • Commercial kit test to detect toxic levels of cyanide in the rumen contents or plant
  • Yellow color changes to brick red in a few minutes (in airtight glass jar)
53
Q

Diagnosis?

A
  • History of consuming cyanogenic plants, bright red mm, and odor of cyanide are indicative of cyanide toxicosis
  • Chemical analysis confirms diagnosis
54
Q

DDx?

A
  • Carbon monoxide (causes bright red blood)
  • Hydrogen sulfide
  • Nitrate
  • Urea
55
Q

How can you differentiate between cyanide toxicosis and hydrogen sulfide poisoning?

A

H2S causes rapid death by inhibition of cytochrome oxidase, but blood and tissues will be dark

56
Q

How can you differentiate between nitrate and cyanide toxicity?

A

Nitrate can cause rapid death (with little exposure), but the blood is chocolate brown colored

57
Q

How is urea poisoning similar/different from cyanide poisoning?

A

Urea may cause rapid death with few lesions, but causes severe colic, nervous and behavioral effects, and the odor of ammonia in the rumen

58
Q

Treatments?

A
  • Sodium nitrite 20% IV at 10-20mg/kg
  • Sodium thiosulfate orally
  • Oxygen therapy is beneficial in addition to nitrite-thiosulfate
  • Vinegar (4L) in 12-20 L cold water orally to slow microbial hydrolysis
  • Mineral oil as a laxative
59
Q

How does sodium nitrite work as a treatment?

A
  • 20% IV at 10-20mg/kg
  • Immediately improves perfusion by causing vasodilation
  • Causes methemoglobin which can bind the CN- and reactivate cytochrome oxidase (too slow to account for the rapid improvement)
60
Q

How does sodium thiosulfate work as treatment?

A
  • 20% IV at 600mg/kg (?)
  • Converts CN- to thiocyanate (SCN) which is less toxic and is excreted in urine

Toxicology (22 decks)

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